The Patient:
Samba is a 45-year-old African man originally from Congo (now living in San Diego) who had been healthy and not on any medications for most of his life. He was admitted to the emergency room recently because he had been exhibiting classic symptoms of diabetes (excessive thirst, urination, and weight loss) for about two months. He lost 35 pounds during this short time!
Samba does not have any known family history of diabetes. He did not feel bad when he was admitted to the ER, and his physical exam did not reveal anything abnormal though he did have abdominal obesity. Routine lab results were normal, except for a markedly elevated glucose value of over 400 mg/dL and severe ketosis consistent with DKA (diabetic ketoacidosis). His triglycerides were high at 300mg/dL.
The Problem:
Samba was admitted to the ICU and given IV fluids and insulin, which is the protocol for patients in DKA. He felt fine at all times and did not understand what all the fuss was about. His blood pressure and other vital signs were normal, as were his kidney function tests.
During his hospital stay, it remained unclear whether Samba had type 1 or type 2 diabetes. The overall assessment leaned toward T2D because he had abdominal obesity and no other symptoms except high blood sugars and high triglycerides. However, he presented in DKA with profound ketones, which for sure is seen as being related to type 1.
After Samba went home from the hospital, his insulin requirements continuously decreased from 90 units per day until he eventually tapered off insulin completely when his glucose control normalized. At his follow-up doctor’s visit, there was a discussion about whether Samba might have something called Flatbush Diabetes.
What Is Flatbush Diabetes?
Flatbush Diabetes, also known as Ketosis-Prone Diabetes (KPD), is a unique subtype of diabetes that has gotten more attention in recent years. This condition, initially found among African American patients in the Flatbush neighborhood of Brooklyn, presents with characteristics of both type 1 and type 2 diabetes, leading to diagnostic challenges and requiring a tailored approach to management.
What Are the Symptoms of Flatbush Diabetes?
People with Flatbush Diabetes often present with symptoms of DKA, including polyuria (frequent urination), polydipsia (excessive thirst), significant hyperglycemia (high blood sugars), weight loss, nausea, vomiting, and abdominal pain. This presentation can be misleading, as it mimics DKA in type 1 diabetes. However, the lack of autoimmune markers and the presence of significant insulin resistance (often associated with obesity) suggest an alternative diagnosis. Flatbush Diabetes predominantly affects people of African, African-Caribbean, and Hispanic descent. The prevalence of this condition highlights the importance of considering ethnic and genetic factors in the diagnosis and treatment of diabetes.
What Are the Causes of Flatbush Diabetes?
The short answer is, we don’t really know. It is thought to involve a transient dysfunction of the pancreatic beta cells, leading to a temporary loss of insulin production. Unlike in type 1 diabetes, this dysfunction is not due to autoimmune destruction. Instead, it may be triggered by things like severe stress, infection, or a combination of genetic predisposition and environmental influences.
How Is Flatbush Diabetes Diagnosed?
Key criteria include the presence of DKA at onset, the absence of autoimmune markers (such as GAD antibodies and islet cell antibodies), and the ability to eventually discontinue insulin therapy while maintaining good glycemic control, which is atypical for type 1 diabetes.
How Is Flatbush Diabetes Treated?
The management of Flatbush Diabetes requires a specialized approach that addresses both the acute and chronic aspects of the disease. Initially, treatment focuses on resolving DKA through IV fluids, insulin, and close monitoring of electrolytes. Once the acute episode is managed, the treatment strategy shifts to maintaining long-term glycemic control.
Many people with Flatbush Diabetes can achieve good glycemic control without insulin after the initial treatment period. Nutrition, exercise, oral medication, and regular blood sugar monitoring are essential components of long-term management.
Samba’s insulin autoantibodies were negative, so at this point the common sense thing to do is to promote healthy living in his eating and exercise habits in addition to providing education about diabetes and his condition specifically.
The Takeaway:
Flatbush Diabetes, or Ketosis-Prone Diabetes, is a type of diabetes that initially blurs the lines between type 1 and type 2, but it is a form of type 2 diabetes. Its unique characteristics, including the acute onset of DKA without autoimmune markers and the potential for insulin independence, highlight the diversity within the spectrum of diabetes. As research continues to uncover the causes and intricacies of this condition, healthcare providers must remain attentive and adaptable, ensuring that people receive the most accurate diagnosis and effective treatment possible.
So once sugar normalizes and insulin is no longer needed, is the medication plan similar to the Type 2 plan with Ozempic and metformin?
If the blood sugars do not normalize, then the treatment plan is the same for type 2s per the ADA algorithm. We have a video on recommended treatments for type 2 here: https://www.youtube.com/watch?v=muoFDJfg7Nk
So Flatbush Diabetes is a transient dysfunction of beta cells, resulting in complete insulin deficiency, that leads to DKA, and after the acute stressor, it usually resolves back to normal. This case is fascinating because these patients can go back to being normal! while those who are typically Type 1 never actually return to baseline and gradually lose their beta cell function,
The exciting thing about this case is the reason behind the difference in both presentations and why they might be different?
I feel it sounds quite similar to the case of De Quervain thyroiditis where there is transient dysfunction of thyroid!
where there is a state of transient dysfunction followed by the gradual recovery of thyroid function or in some cases progressing to permanent hypothyroidism.
Really very fascinating case!